Insomnia - American Academy of Sleep Medicine
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Insomnia
Placeholder – chapter table of contents
An insomnia disorder is defined as a persistent difficulty with sleep initiation, duration, or consolidation
that occurs despite adequate opportunity and circumstances for sleep and results in concern,
dissatisfaction, or perceived daytime impairment, such as fatigue, decreased mood or irritability, general
malaise, or cognitive impairment. Among adults with insomnia disorder, sleep complaints typically include
difficulties initiating or maintaining sleep. Among infants and young children, the complaint is voiced by a
caregiver and may also include bedtime resistance and an inability to sleep independently without
caregiver intervention.
Concerns about associated wake time impairment attributed to the nocturnal symptoms are referred to
as daytime impairment. However, in some circumstances, such as shift work, the wake hours and impact
of poor sleep may occur at night. Among adults with insomnia disorder, daytime impairment may impact
social, familial, vocational, or educational functioning and reduce quality of life. Among children, it may
also lead to inattention and cognitive deficits as well as behavioral and mood disturbances that impair
daily functioning at school, at home, and in social situations. Other daytime symptoms may include muscle
tension, palpitations, headache, and fatigue. Although less common and often confused with fatigue,
daytime sleepiness, when present, may increase the risk for motor vehicle and occupational accidents. In
the absence of reported or observed daytime impairment or dissatisfaction with sleep, individuals who
describe prolonged sleep latency, recurrent or prolonged awakenings, or restricted sleep duration are not
regarded as having an insomnia disorder that warrants clinical attention, other than education and
reassurance.
Insomnia symptoms often accompany comorbid medical illnesses, mental disorders, and other sleep
disorders. Insomnia symptoms may also arise with the use, abuse, or exposure to certain substances. A
separate insomnia disorder diagnosis is warranted when the insomnia symptoms are persistent and result
in distress or impairment.
The insomnia disorder nosology presented in ICSD-3 and maintained in this text revision represents a
marked departure from the prior International Classification of Sleep Disorders, 2nd Edition classification
system regarding its conceptual framework. The previous insomnia nosology of the International
Classification of Sleep Disorders promoted the concept that insomnia can exist as a primary sleep disorder
or arise as a secondary form of sleep disturbance related to an underlying primary psychiatric, medical, or
substance use disorder. However, differentiation between primary and secondary subtypes is difficult, if
not impossible. More importantly, even when another condition initially causes the insomnia, it often
develops into an independent disease entity that merits clinical attention. Evidence suggests that
1insomnia disorder, if left untreated, may adversely affect the outcome, and increase the risk of recurrence
of comorbid conditions. Moreover, it appears that, in some cases, treatment of the insomnia disorder
may improve the outcome of both the sleep disturbance and the comorbid conditions. Given these
observations, insomnia disorder seems best viewed as a comorbid disorder that warrants separate
treatment attention.
In addition to the primary vs. secondary insomnia distinction, prior editions of the International
Classification of Sleep Disorders delineated multiple putative “primary insomnia” diagnostic subtypes.
Specifically, the original 1990 version of the International Classification of Sleep Disorders and the
International Classification of Sleep Disorders, 2nd Edition, described primary insomnia subtypes such as
psychophysiological insomnia, idiopathic insomnia, inadequate sleep hygiene, paradoxical insomnia, and
behavioral insomnia of childhood as discrete diagnostic entities. However, experience suggests that, in
practice, it is rare to encounter patients who meet the diagnostic criteria for one of these subtypes
exclusively. Moreover, many of the diagnostic criteria delineated for these subtypes represent generic
characteristics of insomnia (e.g., engaging in sleep-disruptive habits, underestimating sleep time,
demonstrating evidence of conditioned arousal), per se, and do not facilitate discrimination among these
subtypes or between these subtypes and those presumed to have “secondary” forms of insomnia.
Moreover, both clinical experience and a growing body of empirical findings have shown that the
diagnostic distinctions advocated by previous versions of the International Classification of Sleep
Disorders are difficult to ascertain reliably and are of questionable validity. Given such considerations, the
current manual abandons the previously employed complex and highly specific insomnia classification
scheme described by the original International Classification of Sleep Disorders and the 2nd Edition in
favor of a more global and defensible nosology.
The chapter includes three diagnostic categories for insomnia: chronic, short-term, and other insomnia
disorders. Chronic insomnia disorder is characterized by chronic sleep-onset or sleep-maintenance
complaints with associated daytime impairment. The diagnosis is reserved for individuals whose sleep
difficulties exceed minimal frequency and duration thresholds associated with clinically significant
morbidity outcomes. Short-term insomnia disorder is characterized by sleep/wake difficulties that fail to
meet the minimal frequency and duration criteria of chronic insomnia disorder but are associated with
clinically significant sleep dissatisfaction or perceived daytime impairment. A diagnosis of other insomnia
disorders should be assigned in rare cases that fail to meet criteria for chronic or short-term insomnia
disorder yet have sufficient symptoms of insomnia to warrant clinical attention. Finally, while symptoms
of insomnia in childhood and adolescents share some commonality with characteristics of adult insomnia
disorder, there are unique features that characterize the disorder in younger patients. Moreover, there is
substantial variation in the defining characteristics of insomnia disorder within this young age group. The
section on Developmental Issues highlights these features.
Chronic Insomnia Disorder
ICD-9-CM code: 307.42
2ICD-10-CM code: F51.01
Alternate Names
Historically the literature has used the following terms: primary insomnia, secondary insomnia, comorbid
insomnia, disorder of initiating and maintaining sleep, behavioral insomnia of childhood, sleep-onset
association disorder, limit-setting sleep disorder.
Diagnostic Criteria
Criteria A-F must be met
A. The patient reports, or the patient’s parent or caregiver observes, one or more of the following:1,2
1. Difficulty initiating sleep.
2. Difficulty maintaining sleep.
3. Final awakening earlier than desired.
4. Resistance to going to bed on an appropriate schedule.
5. Difficulty sleeping without parent or caregiver presence or intervention.
B. The patient reports, or the patient’s parent or caregiver observes, one or more of the following
related to the nighttime sleep difficulty:
1. Fatigue/malaise.
2. Impaired attention, concentration, or memory.
3. Impaired social, family, occupational, or academic performance.
4. Mood disturbance/irritability.
5. Subjective daytime sleepiness.3
6. Behavioral problems (e.g., hyperactivity, impulsivity, aggression).
7. Reduced motivation/energy/initiative.
8. Proneness for errors/accidents.
9. Concerns about or dissatisfaction with sleep.
C. The reported sleep/wake complaints cannot be explained purely by inadequate opportunity (i.e.,
time allotted for sleep) or inadequate circumstances (i.e., safety, darkness, quiet, and comfort)
for sleep.
D. The sleep disturbance and associated daytime symptoms occur at least three times per week.
E. The sleep disturbance and associated daytime symptoms have been present for at least three
months.4,5
F. The sleep disturbance and associated daytime symptoms are not solely due to another current
sleep disorder, medical disorder, mental disorder, or medication/substance use.6 ,7
Notes:
31. Reports of difficulty initiating or maintaining sleep or waking up too early can be encountered in
all age groups. Resistance to going to bed on an appropriate schedule, including resisting age-
appropriate naps, and difficulty sleeping without a caregiver’s presence or intervention are most
commonly seen in children and in adults with cognitive impairment.
2. The assessment of chronic insomnia disorder in children and adolescents should include
information from both the child and their caregiver because the caregiver may not have complete
knowledge about the child’s experience of sleep difficulties, and the child may not have full
awareness of the daytime consequences of their sleep difficulties.
3. Patients tend to use the terms sleepiness and fatigue interchangeably. Therefore, the assessment
of subjective daytime sleepiness requires distinguishing the two symptoms. Fatigue refers to low
physical or mental energy, whereas sleepiness refers to the propensity to fall asleep in conducive
circumstances. Although patients with chronic insomnia disorder may report feeling subjectively
“sleepy,” extensive research indicates that most individuals with chronic insomnia disorder have
low objective daytime sleepiness, as measured by the multiple sleep latency test.
4. Applying the adult frequency and duration criteria for chronic insomnia disorder may not always
be appropriate in the first year of life. It is important to consider developmental sleep norms in
defining this disorder in young children. For example, full-term infants are not expected to sleep
through the night regularly (without caregiver intervention such as soothing or nursing) until they
are three to six months of age. Therefore, the three-month duration criterion suggests that a
diagnosis of chronic insomnia disorder might first be considered at six to nine months of
age. However, sleep/wake patterns that are viewed as problematic by caregivers may begin to
emerge in the first 12 months without meeting the required three-month duration.
5. Some patients with chronic insomnia may experience recurrent episodes of sleep/wake
difficulties lasting several weeks at a time over several years, yet not meet the three-month
duration criterion for any single episode. Nonetheless, a diagnosis of chronic insomnia disorder is
merited in these cases, given the persistent sleep difficulties.
6. Comorbidity does not preclude the independent diagnosis of chronic insomnia disorder. Evidence
has clearly shown that even when a co-occurring disorder has instigated the insomnia, the sleep
disturbance often transforms into an independent, self-sustaining disorder. By the time such a
patient presents with an insomnia complaint to a health care provider, the insomnia is usually
either independent of the comorbidity or shares a reciprocal relationship with it. If another
condition does not solely cause the patient’s sleep/wake complaints, those complaints merit a
diagnosis of chronic insomnia disorder and separate treatment attention.
7. Regular users of hypnotic medications who sleep well when they take the medications should still
be assigned a diagnosis of chronic insomnia disorder. They may present clinically with concerns
about their inability to sleep without sleep medications.
Essential Features
The essential feature of chronic insomnia disorder is a frequent and persistent difficulty initiating or
maintaining sleep that results in general sleep dissatisfaction or perceived impairment, reported by the
4patient or a caregiver. Distress about poor sleep or impairment in family, social, vocational, academic, or
other important functions accompanies the sleep complaint. Furthermore, the sleep disturbance and
associated waking symptoms occur despite having adequate time and circumstances to obtain necessary
sleep.
The sleep complaints that comprise chronic insomnia disorder include difficulties initiating or maintaining
sleep. The latter may consist of waking up during the night with difficulty returning to sleep or having a
final awakening occurring too early, well before the desired rising time. Individuals’ sleep complaints may
also change over time. Those with solely sleep-onset complaints may subsequently develop sleep-
maintenance complaints and vice versa. In addition, those who present initially with mixed sleep-onset
and sleep-maintenance difficulties may later evidence only one or the other of these difficulties.
Complaints about poor-quality, unrefreshing, or nonrestorative sleep often accompany sleep-onset and
maintenance complaints. However, complaints of this nature do not merit a diagnosis of chronic insomnia
disorder in the absence of sleep-onset or maintenance difficulties (see Unresolved Issues and Further
Directions).
The degree of sleep disturbance required to assign a chronic insomnia disorder diagnosis is somewhat
arbitrary in that it relies primarily on an individual’s or a caregiver’s sleep complaints. Moreover, the
degree of sleep disturbance that is clinically significant varies across age groups. Empirical data suggest
that among adults, onset latencies and periods of wakefulness during sleep > 30 minutes typically connote
clinical significance. Early morning awakening typically entails the termination of sleep at least 30 minutes
before the desired rising time and a concomitant reduction in total sleep time compared with the usual
premorbid sleep pattern. However, the exact time at which early morning awakenings occur may vary
considerably as a function of usual bedtimes. For example, a complaint of final awakening at 4:00 a.m.
and a desire to sleep more is likely to connote clinical significance when the usual bedtime is 11:00 p.m.
but not when it occurs at 9:00 p.m. There are fewer empirical data concerning thresholds for sleep-onset
latency and frequency of night awakenings in infants and children, as these are age-dependent. Among
very young children, clinical significance also depends on the level of caregiver involvement needed for
the child to sleep.
Qualitative research indicates that adults experience chronic insomnia disorder as a 24-hour problem and
report multiple waking symptoms. Common waking symptoms include fatigue, reduced motivation,
concentration, attention, and memory functioning, and irritability or low mood. Complaints of subjective
daytime sleepiness need to be distinguished from fatigue. Whereas fatigue manifests mainly as a lack of
mental or physical energy and desire to reduce or limit activity levels, subjective sleepiness is
characterized by a reduced level of alertness. Despite a desire to nap, many individuals with insomnia are
unable to do so. However, unintentional dozing, primarily in the evening, may be present. Frequent,
involuntary daytime sleep episodes are more characteristic of other types of sleep disorders such as sleep-
related breathing disorders, narcolepsy, idiopathic hypersomnia, or insufficient sleep syndrome.
Individuals with insomnia also do not exhibit objective sleepiness, as indicated by their longer latency to
sleep onset on the multiple sleep latency test compared to age-matched healthy sleepers with similar
sleep duration. Reports of reduced performance at work or school or impaired social functioning are also
5common. Some affected individuals attribute errors or accidents at work to their sleep difficulties. Somatic
symptoms such as headaches or gastrointestinal dysfunction are occasionally attributed to ongoing sleep
difficulties. Some evidence indicates that the experience of difficulties with both initiating and maintaining
sleep is associated with more significant daytime impairment than the experience of either one of these
nocturnal symptoms alone.
Although transient and episodic forms of insomnia occur, the clinically significant daytime consequences
of a chronic insomnia disorder and the longer-term morbidity outcomes typically develop when the sleep
difficulties occur at least three times per week and persist for at least three months. For this reason, these
frequency and duration criteria must be met to assign a chronic insomnia disorder diagnosis (see Criteria
Notes 4 and 5 regarding exceptions to the duration criterion). More acute and episodic forms of insomnia
may cause significant distress and functional impairment and require clinical attention. Cases that meet
all criteria except the frequency or duration criteria for chronic insomnia disorder should be assigned a
diagnosis of short-term insomnia disorder.
Chronic insomnia disorder can occur in isolation, although it is commonly comorbid with a mental or
medical disorder, another sleep disorder, or substance use. Insomnia symptoms can be solely due to a
comorbidity (e.g., patients with obstructive sleep apnea and complaints of repeated awakenings that
resolve with positive airway pressure). However, as noted above, the symptoms often evolve into a
chronic insomnia disorder that is at least partially independent from the comorbidity and requires
independent assessment and treatment.
Associated Features
Individuals with chronic insomnia disorder typically note feelings of reduced well-being, general malaise
during the day, physical tension at night, and physiological, cognitive, or emotional hyperarousal at night.
Complaints such as: “I can’t shut my mind off” or feeling “wound up” or anxious often characterize the
cognitive and emotional hyperarousal, respectively. In addition, excessive focus on and worry about
ongoing sleep difficulties and their associated daytime consequences are common. Thoughts about
ongoing sleep difficulties may occur throughout the day and may be amplified as bedtime approaches.
Performance anxiety about sleep is common. Anxious thoughts and worries experienced by individuals
with chronic insomnia disorder often focus on the sleep difficulty, including concerns about potential
consequences of poor sleep. A comorbid anxiety disorder may be present when anxiety and worry are
more pervasive and not solely focused on sleep problems. However, even in the absence of anxiety
disorders, rumination about events of the day or anxious thoughts about a future event may make it
difficult to sleep. Whereas for good sleepers, the bed and bedroom are cues for sleep, the sleep
environment becomes a cue for wakefulness for many with chronic insomnia disorder. Such individuals
may fall asleep easily in settings outside of their bedrooms when not trying to sleep but show a pattern
of cognitive and physiological arousal when lying down in their beds intending to fall asleep. Some patients
with this pattern may report sleeping better when away from home. Unlike good sleepers, for whom sleep
is an automatic process, individuals with chronic insomnia disorder often express conscious intentions
6and excessive effort to sleep, only to find sleep difficult to initiate under such circumstances. They tend
to have the same experience when trying to nap and are typically unable to do so.
In infants and toddlers, sleep difficulties can also manifest as difficulty settling into or sustaining naps. In
children, daytime behavioral problems, mood dysregulation, and limit-setting difficulties during the day
may accompany the sleep disturbance. In addition, the nighttime sleep disturbance often results in poor
caregiver’s sleep and associated daytime impairment. Marital conflicts about responding to or intervening
with the child’s ongoing sleep problem may arise. Caregivers may also develop negative feelings toward
the child who disrupts their sleep and demands attention during the night.
Clinical and Pathophysiological Subtypes
Previous nosology’s have described various clinical and pathophysiological subtypes of chronic insomnia
disorders. The American Psychiatric Association’s Diagnostic and Statistical Manual, 4th Edition, Text
Revision (DSM-IV-TR) and the International Classification of Sleep Disorders, 2nd Edition described
independently occurring or primary forms of insomnia. Within DSM-IV-TR, the global term, primary
insomnia, is applied to all forms of insomnia that are not better explained by a coincident psychiatric,
medical, or substance use/abuse disorder. The International Classification of Sleep Disorders, 2nd Edition
delineated multiple primary insomnia subtypes. For reasons described in the introduction and below,
ICSD-3 abandoned this detailed classification and listed all presentations within a single diagnosis of
chronic insomnia disorder. Thus, the ICSD-3-TR does not support classification into subtypes but retains
descriptions below to illustrate settings in which chronic insomnia disorder may arise and for educational
and research purposes.
Psychophysiological insomnia is characterized primarily by heightened arousal and learned sleep-
preventing associations that result in a complaint of insomnia. Patients presumed to have this type of
insomnia often have sleep difficulty when trying to sleep in their usual sleep setting at home but may fall
asleep easily in a novel sleep setting or when not trying to sleep. They also demonstrate an excessive focus
on and worry about sleep and suffer from elevated levels of cognitive and somatic arousal, particularly at
bedtime.
Idiopathic insomnia is characterized by a longstanding complaint of sleep difficulties with insidious onset
occurring during infancy or early childhood. It is presumed to arise in infancy or early childhood without
discernible cause and persist over time without sustained periods of remission. Given its early onset,
stability over time, and lifelong course, this disorder is thought to result from either genetically
determined or congenital aberrations in the sleep-inducing or arousal systems in the brain. However, no
consistent genetic markers or neural pathology have been identified among those presumed to suffer
from this condition.
Paradoxical insomnia, which has previously been called sleep state misperception, is characterized by a
complaint of severe sleep disturbance despite objective evidence of relatively normal sleep initiation,
7maintenance, and duration. Those presumed to have this form of sleep difficulty have a marked
propensity to underestimate the amount of sleep they are obtaining. Essentially, they perceive much of
the time they are asleep as wakefulness. Some studies using neuroimaging or sleep
electroencephalograph (EEG) spectral analysis techniques have suggested that an altered sleep/wake
arousal system may explain the apparent mismatch between their conventional objective sleep measures
and subjective sleep reports.
Inadequate sleep hygiene is presumed to result from or be sustained by daily living activities that are
inconsistent with the maintenance of good-quality sleep and normal daytime alertness. These practices
include daytime napping; maintaining a highly variable sleep/wake schedule; routinely using sleep-
disruptive products (caffeine, tobacco, alcohol) too close to bedtime; engaging in mentally or physically
activating or emotionally upsetting activities too close to bedtime; routinely using the bed and bedroom
for activities other than sleep; and failing to maintain an environment that is conducive to sleep.
Behavioral insomnia of childhood is presumed to result from improper sleep training or limit-setting by
parents or caretakers. Several subtypes have been described within this broader diagnosis. Sleep-onset
association type is characterized by the child’s dependency on specific stimulation, objects, or settings for
initiating or returning to sleep following an awakening; sleep onset is significantly delayed in the absence
of these conditions. Limit-setting type is characterized by bedtime stalling or bedtime refusal resulting
from inadequate limit-setting by a caregiver. A mixed type characterized by features of sleep-onset
association difficulties and bedtime resistance represents the third subtype within this diagnostic
category.
The DSM-IV-TR and International Classification of Sleep Disorders, 2nd Edition also described several so-
called secondary insomnias arising from co-occurring primary or causative conditions. Among these are
the following:
Insomnia due to (another) mental disorder is caused by or secondary to a co-occurring psychiatric
condition. Insomnia is a common complaint among those with mental disorders, particularly among
patients with mood disorders and anxiety disorders. Likewise, psychotic spectrum disorders and various
Axis II (personality) disorders are frequently associated with sleep disturbance. Among those individuals
presumed to have insomnia due to a mental disorder, insomnia has historically been regarded as a
secondary symptom caused by the mental disorder itself.
Insomnia due to (a) medical condition is caused by or secondary to a co-occurring medical condition. Like
mental disorders, many medical conditions may have an ongoing insomnia complaint associated with
them. In particular, those conditions that cause some form of persistent pain or discomfort, mobility
limitation, or breathing disturbance commonly have insomnia complaints accompanying them. Among
those individuals presumed to have insomnia due to a medical disorder, insomnia has historically been
regarded as a secondary symptom caused by the medical disorder itself.
8Insomnia due to drug or substance is caused by or secondary to use of or withdrawal from a drug or
substance. Many forms of prescription and nonprescription medications, street drugs, and other
commonly used substances may produce sleep disturbances during periods of use or upon withdrawal.
Given these effects, insomnia complaints may arise during periods when these substances are used or
following their discontinuance. Among those individuals presumed to have insomnia due to drug or
substance, insomnia has historically been regarded as a secondary symptom caused by the drug or
substance itself.
Research has provided minimal support for the reliability and validity of most of these specific subtypes.
It is also difficult to discriminate among them in clinical practice. Many of the defining features of these
previously defined subtypes, such as conditioned arousal, poor sleep hygiene practices, and
underestimation of sleep duration, are ubiquitous among individuals with chronic insomnia disorder. They
are therefore not specific to one subgroup. There is also limited support for an insomnia subtype due to
another medical or psychiatric disorder. Although these conditions may precipitate sleep difficulties, the
sleep difficulties are maintained over time by compensatory behaviors and thoughts and result in daytime
impairment. When this occurs, the symptoms are independent of the comorbid disorder and instead
become a self-sustaining insomnia disorder that impacts and is impacted by the co-occurring disorder. As
a result, it is practically impossible to draw firm conclusions about the direction of causality between
insomnia and such co-occurring conditions.
The International Classification of Sleep Disorders, 2nd Edition additionally delineated the separate
pediatric diagnosis, behavioral insomnia of childhood, characterized by sleep difficulties resulting from
inappropriate sleep associations or inadequate limit setting by parents or caregivers. As a descriptive
entity, this designation remains clinically useful when treating young children because it defines etiologic
factors that can guide the formulation of targeted behavioral intervention strategies. However, there is
limited empirical support for this diagnostic subtype. Moreover, inappropriate sleep-onset associations
and inadequate limit-setting may be observed across the age spectrum. For example, adults with chronic
insomnia disorder may report intolerance for quiet and dark environments and may be unable to fall
asleep unless the television is on. Similarly, limit-setting issues may be manifested among cognitively
impaired adults when caregivers fail to set limits on daytime napping that predisposes to disruptive
awakenings and night wandering. Nevertheless, as discussed earlier, there are unique features of chronic
insomnia disorder experienced by children and adolescents that are discussed in the Developmental
Issues section below.
In addition to these various subtypes, a distinct subtype of insomnia with objectively short sleep duration
has been described. This patient group is characterized by insomnia complaints, along with an objectively
documented average sleep time of fewer than six hours per night and elevated morbidity risk. Although
evidence supporting this chronic insomnia disorder subtype is growing, it is premature to delineate a
separate insomnia category for this presentation.
Given these considerations, the ICSD-3 has chosen a more global and defensible approach for diagnosing
those with chronic insomnia complaints. Specifically, the single diagnosis of chronic insomnia disorder
9applies to all patients who have persistent and frequent insomnia complaints, whether they occur in the
presence or absence of a potentially sleep-disruptive comorbid psychiatric illness, medical disorder, or
pattern of substance use.
Demographics
The complete clinical syndrome of chronic insomnia disorder occurs in about 10% of the population, but
the prevalence of transient insomnia symptoms is much higher (30% to 35% of the population). Chronic
insomnia disorder is more common in women; those with medical, psychiatric, or substance use disorders;
and in people in lower socioeconomic strata. A substantial majority of people with insomnia also
experience an intrusive co-occurring medical or psychiatric condition. About 30% of people with chronic
insomnia disorder also have obstructive sleep apnea, and nearly 40% of people with obstructive sleep
apnea also have insomnia symptoms. Chronic insomnia disorder may occur at any age but is more
commonly diagnosed in older adults, in part due to age-related cognitive decline/dementia, deterioration
in sleep continuity, and an increase in medical comorbidities and medication use that increase insomnia
risk.
Chronic insomnia disorder is estimated to occur in 10% to 30% of children, depending on the exact
definition used and age. Specific subgroups of children, including those with chronic medical disorders,
psychiatric comorbidities, and neurodevelopmental disorders such as attention-deficit/hyperactivity
disorder and autism spectrum disorder (ASD) have a higher prevalence of insomnia symptoms. For
example, current data suggest that up to 80% of pediatric patients diagnosed with ASD have significant
sleep complaints. There is also a high prevalence of chronic insomnia disorder among children and
adolescents with genetic (e.g., Smith-Magenis and Angelman syndromes) or acquired (e.g., fetal alcohol
spectrum) disorders. Studies on adolescents indicate prevalence rates of 3% to 39%, depending on the
diagnostic criteria utilized and the age range studied. Recent estimates employing DSM-5 criteria for the
16 to 18-year-old age group are 12% in boys and 18% in girls.
Predisposing and Precipitating Factors
Predisposition refers to longstanding vulnerability to developing an insomnia disorder. Individuals who
have difficulty sleeping during stressful times or report being habitual light sleepers appear to have an
elevated propensity to develop chronic insomnia disorder. Prior transient episodes of sleep difficulties
elevate the risk for subsequent development of a chronic insomnia disorder. A personal tendency to be
excessively anxious or overly concerned about health, general well-being, or daytime functioning may
serve as predisposing characteristics. Indeed, individuals with chronic insomnia disorder often display an
excessive preoccupation with daytime consequences of poor sleep and devote particular effort to what
they assume to be sleep-promoting practices. A history of trauma can also predispose individuals to
develop chronic insomnia disorder due to increased hypervigilance.
10Heritability is a strong predisposing factor for insomnia. Concordance rates among monozygotic twins are
higher than in dizygotic twins. The rate of insomnia in first-degree relatives of people with insomnia
symptoms is higher than in first-degree relatives of people without insomnia. There is an estimated 40%
genetic influence in symptomatic insomnia. The genetic weight specifically in chronic insomnia disorder
has yet to be determined.
Concerning the pediatric age group, caregivers who have unrealistic sleep expectations for their children
may predispose them to insomnia by putting them in bed too early or assigning them too much time in
bed each night. Similarly, parents and caregivers of young children who fail to set limits on the child’s
sleep behaviors also create an unstructured sleep environment that predisposes young children to
develop chronic insomnia disorder.
Precipitating factors are immediate instigators of sleep disturbance. Job-related or financial stress and
factors such as the death of a loved one, divorce, a marked change in work schedule, job loss, and other
significant life changes are often precipitating circumstances for chronic insomnia disorder. Other
contributing factors include unstable home situations, safety concerns, and physical, mental, or sexual
abuse or domestic violence exposure. Mild-to-moderate stressors can also precipitate insomnia.
Psychiatric conditions, particularly mood and anxiety disorders, may precipitate chronic insomnia
disorder. Likewise, comorbid restless legs syndrome or medical disorders such as gastroesophageal reflux
disease or conditions that result in chronic pain, breathing difficulties, or immobility can also lead to
chronic insomnia disorder. Consumption of a large quantity of alcohol at night may contribute to
insomnia, particularly sleep-maintenance problems. A pattern of alcohol dependence/abuse, excessive
use of caffeine (such as energy drinks) or other stimulants, and excessive evening use of electronic media
may increase the risk for chronic insomnia disorder. This latter group of risk factors is prevalent among
adolescents.
In children, life stresses that impact sleep include the development of a medical or psychiatric illness;
physical, emotional, or sexual abuse; death of a parent; exposure to negative parental interactions,
separation, or divorce; and placement in an alternate care setting, such as foster care.
In many cases, predisposing or precipitating factors cannot be identified. This is particularly true in
longstanding insomnia.
Familial Patterns
The familial pattern of insomnia is not well documented. However, family studies indicate that the
prevalence of insomnia is higher among first-degree relatives of people with chronic insomnia disorder
(~35-55%) than among good sleepers. Mothers are the most frequently afflicted first-degree relative.
Evidence from several twin studies indicates that heritability estimates for insomnia fall in the moderate
range for adults and younger children but are somewhat lower for adolescents. Genetic influences are
more important in the etiology of insomnia symptoms for females than males and are largely stable over
11time. Candidate gene approaches have identified genetic variants across numerous systems, but few have
been studied in detail, and findings have often not been replicated. Genome-wide association studies of
chronic insomnia disorder and individual nocturnal insomnia symptom phenotypes using multiple biobank
databases (UK Biobank, Partners Biobank, HUNT study) have identified several insomnia-related genes,
including MEIS1, CACNA1C, and RBFOX3. These findings have been replicated across different
populations. Evidence for shared genetic factors between insomnia and a range of health conditions,
including psychiatric and cardiometabolic disorders, has been consistently identified. However, further
work is needed to determine the extent to which familial aggregation represents shared genetic
predisposition, shared environment, learned behavior (e.g., by observations of parental behavior), or a
by-product of psychopathology.
Onset, Course, and Complications
Onset may be insidious or acute. In the former case, individuals may report insomnia symptoms in early
life or young adulthood. Among adults, the onset of chronic insomnia disorder often has a clear
precipitating major life event (see Predisposing and Precipitating Factors). However, in some cases, the
origin of insomnia cannot be identified.
The course of insomnia can be episodic or persistent. The specific type of sleep complaint may also change
over time. Individuals who complain of difficulty falling asleep at one time may later complain of difficulty
maintaining sleep and vice versa (see Essential Features). Although short-term insomnia caused by a clear
precipitating event or situation may remit when the precipitating event subsides or the individual adapts
to it, sleep difficulties may persist over time even after the initial triggering factor has disappeared. When
left untreated, persistent insomnia disorder may worsen over time. Concerns about sleep and daytime
impairments, apprehension about poor sleep, and engagement in counter-productive behaviors may
worsen sleep disturbance. Chronic insomnia disorder can also follow an intermittent course, with
recurrent episodes of sleep difficulties that worsen with life stresses. In general, individuals with chronic
insomnia disorder experience night-to-night variability of symptoms, with an occasional good night’s sleep
interspersed with several nights of poor sleep. Approximately 70% of individuals with insomnia at a given
time report insomnia a year later, and 50% still have insomnia three years later.
Complications of persistent insomnia include increased risks for new onset or recurrence of depressive
and other psychiatric disorders, as well as suicidality. Chronic insomnia also confers risk for work disability
and prolonged use of prescription or over-the-counter sleep aids. In addition, there is some evidence for
increased risk of hypertension among individuals with chronic insomnia disorder who have short
objectively measured sleep duration, defined as under 6 hours.
Among children, chronic insomnia disorder may have its onset at any time from late infancy through the
childhood years. The course of chronic insomnia disorder in young children varies and depends on the
reasons for the sleeplessness. When limit-setting factors and negative sleep associations resolve, sleep
often improves. In adolescence, caregivers may cease to set limits, leading some teens, particularly those
12with eveningness chronotype, to maintain a delayed or irregular sleep schedule. In turn, this may
precipitate or exacerbate sleep difficulties, sleep loss, and associated consequences. While studies suggest
that young children with early onset insomnia are more likely to have persistent or recurrent insomnia
throughout childhood, the trajectory linking childhood insomnia to adult insomnia is less clear and
requires further study.
Developmental Issues
Several unique developmental issues are highly relevant to the conceptualization of chronic insomnia
disorder in infants, children, and adolescents.
The first involves the importance of viewing insomnia symptoms within the context of age-related sleep
norms and the developmental trajectory of changes in sleep and circadian biology across this age
spectrum. During childhood, there is a gradual decline in the normative duration of nocturnal and daytime
sleep. Early childhood is associated with a decrease in the frequency of normal nighttime awakenings
(paralleling the gradual lengthening of the ultradian cycle). Later in childhood, bedtime is progressively
delayed, and, by adolescence, circadian and behavioral processes contribute to increased prevalence of
eveningness chronotype. This preference for a later bedtime, in turn, contributes to shorter sleep duration
on school nights and extended duration on weekends (see below).
Second, developmental progression across domains, including motor milestones, language acquisition,
social/emotional, and cognitive development, all affect the types and manifestations of insomnia across
childhood. For example, developmentally normative separation anxiety and fear of being in the dark may
contribute to children requesting the presence of a caregiver in the bedroom, refusing to sleep in their
own bed or delaying going to bed. In cases where appropriate limits are not set, the child may become
dependent on the presence of a caregiver for initiating sleep at the beginning or middle of the night. In
the absence of these conditions, both sleep onset at bedtime and return to sleep after normal night
awakenings are often significantly prolonged. If the conditions associated with falling asleep are
reestablished, the child usually resumes sleep relatively quickly. Because maladaptive sleep-onset
associations are highly prevalent among young children, a diagnosis of chronic insomnia disorder is
merited only when both of the following conditions are present: (1) the associations are prolonged,
demanding and typically require caregiver intervention/presence (e.g., extended rocking or car rides), and
(2) in the absence of these specific conditions, sleep onset is significantly prolonged, or night awakenings
are extended and disruptive.
Third, caregivers’ behaviors, bedtime interactions, and expectations regarding appropriate child behavior
and definitions of “good parenting” can impact chronic insomnia disorder. These beliefs and behaviors, in
turn, often reflect the culture and environment of the family. Caregivers’ issues are relevant to chronic
insomnia disorder across childhood and adolescence as well as in adults who need care for daily function.
A significant caregiver issue relates to limit setting. Inadequate limit setting occurs when caregivers
institute inadequate developmentally-appropriate limits or when the limits are instituted inconsistently
or unpredictably. Consequences of poor limit setting manifest as stalling or refusing to go to bed or return
13to sleep during the night. While most commonly presenting as a sleep-onset complaint, limit-setting sleep
problems may also result in prolonged nocturnal awakenings, depending on caregiver response during
the night. In early childhood, limit-setting issues tend to intensify when the child starts climbing out of the
crib or is moved into a bed. In children, as well as in adults with dementia, inadequate limit setting can
also occur when the caregiver permits excessive sleeping during the day or establishes a sleep opportunity
window that is too long. Extended time in bed may lead to difficulty with sleep onset or maintenance,
including fragmented sleep or waking at an undesirably early time in the morning.
Lastly, there are specific developmental factors relevant to chronic insomnia disorder during adolescence.
Adolescents typically seek greater independence from caregivers, resulting in the adolescent’s resistance
to following adult-prescribed recommendations regarding sleep or in caregivers relinquishing oversight of
sleep practices. Both occurrences may contribute to chronic insomnia disorder. In addition, executive
functioning in adolescents is still evolving. As a result, adolescents may engage in numerous sleep-
interfering practices such as spending excessive time and using electronics in bed. Emergent
chronobiological and social factors contribute to a propensity for delaying bedtimes (“eveningness”
preference) compared to pre-pubertal children. Early rise times, dictated by school start times, may
require bedtimes earlier than circadian sleep propensity. Thus, if the adolescent tries to fall asleep at an
earlier bedtime to obtain sufficient sleep, repeated unsuccessful attempts at sleep initiation may
precipitate a chronic insomnia disorder (which may be comorbid with a delayed sleep-wake phase
disorder).
The specific symptoms of chronic insomnia disorder, as well as precipitating and perpetuating factors,
may vary across the adult age range. These changes partly reflect developmental changes across
adulthood, such as a phase delay of endogenous circadian rhythms in adolescence and young adulthood,
a phase advance and increased number of awakenings among healthy older adults, and a breakdown of
circadian rhythms among adults with neurodegenerative disorders. Epidemiological studies confirm that
sleep-onset difficulties and nonrestorative sleep are most common among young adults with chronic
insomnia disorder. In contrast, sleep-maintenance insomnia and early morning awakening are more
common in middle-aged and older adults. Objective daytime sleepiness is uncommon in younger adults
with chronic insomnia disorder but more common in older adults, possibly related to increased prevalence
of other comorbid medical and sleep disorders. Precipitating factors for chronic insomnia disorder may
also change across the adult age range, with medical and medication factors assuming a more significant
role in older adults. Indeed, hypnotic medications are disproportionately prescribed to older adults, often
with limited benefit and the potential for rebound and withdrawal insomnia. Likewise, perpetuating
factors may vary with the life circumstances of adults of different ages. For example, older adults may
spend large amounts of time in bed after retirement, adversely affecting sleep continuity. In addition,
medical disorders, and symptoms (e.g., pain, dyspnea, and impaired mobility), as well as cognitive
impairment, play a more prominent role in the perpetuation of insomnia among older adults. Likewise,
medications for comorbid conditions that have known negative impacts on sleep may contribute to
developing and maintaining a chronic insomnia disorder.
14Pathology and Pathophysiology
Studies of the pathophysiology of chronic insomnia disorder have focused on various dimensions of
hyperarousal during sleep and wakefulness. These studies contrast groups of people with insomnia,
typically those without significant comorbidities, with healthy controls, using a variety of physiological
measures. Many of these studies have small sample sizes and have not been replicated. Collectively these
studies suggest increased physiological arousal among individuals with insomnia, characterized by
measures such as increased heart rate; altered cardiovascular autonomic activity; increased whole-body
metabolic rate; elevated cortisol, adrenocorticotropic hormone, and corticotropin-releasing factor (CRF)
levels (particularly near sleep onset); increased body temperature; and increased high-frequency
electroencephalographic (EEG) activity during non-rapid eye movement (NREM) sleep. Markers of
physiological arousal have been associated with insomnia in children and adolescents, although data are
much more limited than for adults. A few studies have documented alterations in cortisol and
inflammatory markers in pediatric insomnia in both young children and adolescents. These studies imply
heightened sympathetic nervous system and hypothalamic-pituitary-adrenal axis activity across sleep and
wakefulness that perpetuates sleep/wake dysfunction. Some evidence also suggests that physiological
dysregulation may be more evident in specific subgroups of individuals with insomnia (e.g., those with
extreme subjective-objective sleep discrepancies or those with insomnia and short objective sleep
duration). There is also evidence that these findings may not generalize to insomnia comorbid with mental
disorders, which may have different pathophysiological findings. Emerging findings from neuroimaging
and circadian-related studies further suggest that a more complex model than sleep-wake hyperarousal
is needed to fully explain the pathophysiology of insomnia.
No discrete structural brain pathology can be identified in most individuals with insomnia. Patients with
insomnia comorbid with neurological disorders such as stroke, brain trauma, and multiple sclerosis may
have identifiable brain lesions, but insomnia is rarely their sole neurological symptom. Studies have
provided conflicting evidence regarding the finding of reduced hippocampal or anterior cingulate volume,
with most studies reporting negative results.
Objective Findings
Polysomnography (PSG) and the Multiple Sleep Latency Test (MSLT) are not indicated in the routine
evaluation of insomnia; however, they are indicated to rule out other sleep disorders when the clinical
presentation warrants. For example, sleep testing should be considered when symptoms or bed partner
observations of a sleep-related breathing disorder or periodic limb movements during sleep are present.
In addition, patients who present with insomnia symptoms accompanied by excessive daytime sleepiness
may warrant PSG and MSLT testing, particularly if comorbid narcolepsy is suspected. Finally, sleep testing
should also be considered to rule out a comorbid sleep disorder in patients who show acceptable
adherence to trials of well-established insomnia therapies but fail to show adequate treatment response.
In the absence of other sleep disorders, results of PSG monitoring of patients with chronic insomnia
disorder may show increased sleep latency or increased wake time after sleep onset, coupled with
15reduced sleep efficiency in comparison to good sleeper controls. Sleep-onset latency or wake time after
sleep onset often exceeds 30 minutes, although one-hour to two-hour periods of wakefulness in bed are
not uncommon. Sleep duration may also be reduced compared with good sleeper controls. A subset of
insomnia patients sleeps less than six hours per night. Some patients show altered sleep architecture with
an increase in stage N1 sleep and a decrease in slow-wave sleep and REM sleep. Patients with a
pronounced conditioned sleep difficulty in the home environment may show a reverse first-night effect in
the sleep laboratory (i.e., better sleep on the first vs. subsequent recording nights).
Patients with chronic insomnia disorder typically underestimate sleep duration and overestimate sleep
latency and awakenings. In contrast, good sleepers tend to overestimate sleep duration and
underestimate sleep latency and awakenings relative to PSG. However, some patients with chronic
insomnia disorder demonstrate a marked subjective-objective discrepancy. Despite significant subjective
complaints, PSG reveals age-appropriate sleep duration and an absence of sleep-onset or maintenance
difficulties. This presentation of chronic insomnia disorder has previously been categorized as subjective
insomnia, sleep state misperception, or paradoxical insomnia. Some insomnia patients have alterations in
quantitative measures of the sleep EEG compared with individuals without sleep complaints. Specifically,
these patients often show greater power in the high-frequency bandwidths (especially beta) during
wakefulness, NREM, and REM sleep. Some studies have shown that elevated high-frequency power is
especially characteristic of individuals with chronic insomnia disorder with marked subjective-objective
discrepancies in sleep measures, compared to those with obvious objective sleep disturbances or without
sleep complaints.
Young children with chronic insomnia disorder typically show essentially normal sleep during PSG
monitoring when the caregiver is present and appropriate limits are set in the laboratory. Objective
studies of sleep among adolescents have demonstrated mixed findings. Some studies report longer sleep
latency and wake after sleep onset among those with insomnia than those without, while others report
no difference between the two groups.
Serial monitoring with PSG or actigraphy in individuals with insomnia typically shows marked night-to-
night variability in all sleep measures and recorded bed and rising times, compared to good sleepers.
Studies using actigraphy have not found reliable parameters to differentiate people with insomnia from
good sleepers.
Results of the MSLT usually show normal daytime alertness. In several studies, patients with chronic
insomnia disorder have longer mean MSLT values (i.e., less sleepiness) than control subjects, suggesting
hyper-alertness or hyperarousal. A minority of insomnia patients, particularly older adults with chronic
insomnia disorder, have reduced mean MSLT values indicating increased sleepiness. Such a finding should
prompt consideration of other concurrent sleep disorders such as obstructive sleep apnea.
Patients with chronic insomnia disorder can also be differentiated from good sleepers on several other
physiological measures, including cortisol levels and rhythmicity, heart rate/sympathetic activity, blood
pressure, and metabolic rate, among others (see above). Some of these studies find more significant
16physiological abnormalities among insomnia patients with objective short sleep duration and
improvement in some of these parameters with treatment.
Patients with insomnia frequently complain of daytime cognitive impairments. Studies generally support
small to moderate deficits in the focused cognitive domains of complex attention, problem-solving,
episodic memory, and manipulation/retention in working memory.
Finally, an increasing number of structural and functional controlled imaging studies have been conducted
during sleep and wakefulness in insomnia. Findings across these studies provide some support, though
inconsistent, for the hyperarousal model of insomnia. In addition, structural magnetic resonance imaging
(MRI) studies suggest other factors such as gray matter atrophy in the orbitofrontal and temporal areas
of the cortex, precuneus, and hippocampus, and volume increase in the anterior cingulate cortex (ACC) in
patients with chronic insomnia disorder compared to good sleepers. Controlled functional imaging studies
suggest regionally specific alterations of relative glucose metabolism in chronic insomnia disorder.
Specifically, these studies show smaller wake to NREM decreases of relative glucose metabolism in
sleep/wake-regulating regions, including the thalamus, upper brainstem, anterior cingulate, and limbic
cortex. Self-reported and objective sleep disruptions correlate with increased relative metabolism in these
regions. These findings are similar to regional activation patterns during sleep in an animal model of
stress-induced insomnia. Other studies using nuclear magnetic resonance spectroscopy have identified
reduced gamma-aminobutyric acid (GABA) signaling in sleep-regulating regions in insomnia that
correlates with objective measures of sleep continuity. Studies examining task-related changes in blood
flow using blood oxygenation level-dependent functional magnetic resonance imaging (BOLD fMRI)
paradigms have shown reduced activation of specific brain regions in individuals with chronic insomnia
disorder compared with good sleeper controls. Task-related activation changes in the direction of
“normalization” following cognitive behavioral treatment. Studies using newer imaging techniques and
analytic approaches suggest alterations in the structure and connectivity of brain networks in patients
with insomnia compared to good sleepers. Still, there remains a lack of convergent findings between
structural and functional disturbances among insomnia patients, resulting from heterogeneity in sample
populations and methodological approaches.
Differential Diagnosis
Circadian rhythm sleep disorders Sleep initiation problems are present in individuals with delayed sleep-
wake phase disorder (DSWPD). Among those with DSWPD, sleep initiation is consistently later than
desired or required because the individual’s endogenous circadian rhythm is delayed relative to the
desired bedtime. Sleep-onset difficulties develop when they attempt to initiate sleep earlier than allowed
for sleep onset by the delayed endogenous circadian rhythm. Unlike patients with a chronic insomnia
disorder, patients with DSWPD are typically able to fall asleep with less difficulty and sleep a normal
amount of time when sleeping in phase with their delayed endogenous rhythm by selecting late bed and
rising times. By comparison, those with a chronic insomnia disorder are unable to sleep regardless of the
timing of their bed and rise times. Given the prevalence of delayed sleep-wake phase disorder in teenagers
17and young adults, it is essential to consider the possibility of DSWPD as an alternate or comorbid diagnosis
when evaluating individuals from these age groups presenting with sleep-onset difficulties. It is estimated
that a little over half of adolescents with delayed sleep-wake phase disorder have comorbid insomnia
symptoms.
A chronic insomnia disorder that presents as difficulty maintaining sleep with premature morning rise
times should be differentiated from advanced sleep-wake phase disorder. Among those with an advanced
sleep-wake phase disorder, sleep initiation is consistently earlier than desired because the individual’s
endogenous circadian rhythm is advanced relative to the desired sleep schedule. However, total sleep
time is adequate when the individual chooses early bed and rise times that coincide with the advanced
endogenous circadian rhythm. In contrast, those with chronic insomnia disorder may display sleep-
maintenance difficulties with premature morning rise time regardless of the sleep schedule they select.
An early sleep-wake pattern tends to be more common in older adults.
There can be an overlap between chronic insomnia disorder and both delayed and advanced sleep-wake
phase disorders. For example, patients with a delayed sleep pattern may become chronically frustrated
or anxious about their inability to initiate sleep at their desired times. This frustration or anxiety may
disrupt sleep and delay sleep onset well beyond the time supported by the endogenous rhythm. Similarly,
individuals with an advanced sleep pattern may experience early morning awakenings that are even
earlier than dictated by their endogenous rhythm. In such circumstances, both a circadian rhythm sleep-
wake disorder diagnosis and a chronic insomnia disorder diagnosis may apply and should be assigned.
Sleep-disruptive environmental circumstances A variety of environmental factors, including excessive
noise or light and extreme temperatures, will disrupt the sleep of most individuals. Also, sleeping in an
area where there is an imminent threat or danger to one’s safety can be disruptive to sleep. Bed partners
who snore loudly, move excessively during sleep, or have parasomnias may also disrupt one’s sleep. When
an individual reports environmental circumstances that would be regarded as disruptive to the sleep of
most individuals, yet sleep well in another less disruptive environments, a chronic insomnia disorder
should not be assigned. Chronic insomnia disorder only applies when the individual reports sleep difficulty
in the context of a sleep-conducive environment or when the insomnia symptoms show some
independence from the environmental factors. When environmental circumstances are a primary cause
of sleep disturbance, a diagnosis of other sleep disorder may apply.
Chronic insufficient sleep syndrome Chronic insomnia disorder should also be differentiated from
inadequate sleep duration due to work and other responsibilities or social and recreational schedules.
Daytime sleepiness and fatigue typically occur as a result of insufficient sleep. However, when these
individuals allow sufficient time to sleep, they can initiate and maintain sleep easily and for a normal
duration. In contrast, those with chronic insomnia disorder have difficulties initiating and maintaining
sleep and reduced sleep duration despite routinely allotting sufficient time to sleep. Moreover, unless
other comorbid sleep disorders are present, chronic insomnia disorder is not typically associated with the
excessive daytime sleepiness and unintentional daytime sleep episodes often observed in those with
voluntary sleep restriction.
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